Role of abnormal sarcoplasmic reticulum function in atrial fibrillation

Atrial fibrillation is the most common cardiac arrhythmia and is a cause of significant morbidity and mortality if left untreated. Atrial fibrillation has been associated with profound changes in sarcoplasmic reticulum Ca2+ homeostasis, which might contribute to both reduced contractile function and increased arrhythmogenesis in the atria. Studies in human tissue samples and various animal models of atrial fibrillation have revealed changes in both expression levels and post-translational modifications of key Ca2+ handling proteins that may contribute to arrhythmogenesis. In this article, we will focus on the molecular basis of alterations in sarcoplasmic reticulum Ca2+ handling in atrial fibrillation and their potential therapeutic implications.